histopathology of caries :) Flashcards by Cassie Lee

clincial types of cariees

acute
chronic
arrested

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what is acute caries

caries which is extensive

affects flat surfaces of the teeth (ie front of incisors)

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what is chronic caries

occlusal caries

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what is arrested caries

caries has stopped due to a change in environment

part of the mouth has become self cleaning

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what does ground sectons allow us to look at

hard parts of the tooth

cannot preserve soft tissue

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demineralised sections

organic matrix left

cannot see enamel

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normal enamel

prisms
prism borders
cross striations
straie of retizus
surface zone

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straie of retizus

more pronounced incremental lines

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what causes incremental lines

ameloblasts stop and rest and then move in a different direction

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where does demineralisation generally start and why

prism borders
cross straitions
straie of retizus
- have more organic matrix allowing acid to enter

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sites for caries

smooth surface
fissur
root/cementum
recurrent (caries under a restoration)

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types of arrested caries

type 1 and type 2

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what is type 1 arrested caries

advanced dentine lesion becomes self cleaning

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what is type 2 arrested caries

white spot enamel lesion may remineralise

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where does root/cementum caries usually start

ACJ - where enamel meets cementum

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where is root caries seen

proximal and buccal root surfaces

can have multiple lesions on same tooth

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caries on cemntum/dentine

poorly resistance
PDL fibres allow rapid spread to dentine
caries will progress apically due to tubules in dentine

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classifications of pulp pathology

inflammatory

degenerative

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what is inflammatory pulp pathology

pulpitis ie pulp inflammtio

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types of degenerative pulp pathology

fibrosis
calcifications
internal resorption

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forms of pulpitis

acute
chronic
then within these are open and closed

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what is open pulpitis

pulp is open to orla envionrment

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what is closed pulpitis

enamel is still in tact, pulp not exposed

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causes of pulpitis

infection
-dental caries
- cracked teeth
- transient bacteriamia
trauma
physcial, mechanical, chemical

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what happens is the pulp is not treated

die by necrosis

what happens after the pulp begins to die by necrosis

inflammatory process starts at the apex of the root

types of periapicla pathology

``` periapical periodontis (inflammatory) reactive - hypercementosis - ankylosis - osteoscelrosis ```

causes of periapical pathology

infection (vie root canal, periodontium or bacteriamia) | trauma (chemical, physical, mechanical)

what can pulpitis least to

formation of a cyst

what is the earliest evidence of a carious lesion on a smooth surface

white/brown spot

where is a lesion most likey to form on a premolar tooth

below the contact point between teeth where palaque can stagnante and collect

why may lesions be brown instead of white

enamel increases in porosity and then pigment of food wll be absorbed

how can an early carious lesion be fixefd

enamel is still in tact and can be remineralsied - removal of plawue - apply fluride - improve OH

what can happen at the ADJ

laterla spread of caires | acid can spread more easily

what 4 zones are there within the enamel lesion

translucent zone dark zone body of lesion surface zone

what is the largest zone in the enamel lesion

body of lesion

what do the zones relate to

enamel porisity

what zone has the greatest porosity

body

what porosity results in cavitation

20-25% | body can no longer support the surface lesion

how does porosity increase

movement of calcium out of the tooth | hydroxyapitite mineral is being dissolved out of the enamel

translucent zone

advancing edge of lesion small number of large pores demineralisation at the edgeof prisms in 50%of lesions

dark zone

``` 85-85% lesions varible in thickness narrower =more rapid advance more pores but smaller than TZ represents re-precipitation of minerals dissolved out in TZ ```

body of lesion

demineralisatio of prism cores pore volume 20% centre 5% edge some amount of reprecipitation

surface zone

unaffected layer incontact with surface biofilm resisits demineralisation until dentine involved

dynamic process of de/remineralsiation

acid influxes results into demineralisation and movement of CA out fluride favours reminerlisation (calcium moves in)

earliest clinical evidence in enamel fissure caries

white opacit around fissure paerure | may be sticky brown spot

shape of fissure caries and where do they arise and spread

conical lesion with base towards ADJ lesion arise in fissure walls spread at ADJ

how does fissure caries progress into dentine (types)

``` priamry enamel caries - lateral spread at ADJ secondary enamel caries - careis extends backwards early dentine caries - acid diffuses to dentine ```

what respond toether as a compelx

dentine and pulp

how does the dentine and pulp respond to caries

dentine tubules run from ADJ to the pulp | the tubules are closed off in responce

what are defence reactons of plaque acid

tertiary dentine scelrotic entine dead tracts

tertiary dentine

closes off the tubules at the pulp end and make more dentine

sclerotic dentien

fill in the tubules | mineralisation of odontoblast processes

dead tracts

empty tubules sealed at th end and filled with air | odontoblast death

what the the shapeof caries affected by

site | ie fissure vs smooth surface

dental caries before cavitation

acid diffuses through intact porous enamel | pulp dentine unit repspods

what are the two main zones before cavitation

``` scelortic zone (around the outside) body of lesion (deminerlised) ```

how does cavitation occur

surface enamel no longer able to structurally support itself | (carious enamel collapses_

what happens after bactera has entered the dentine

1st wave - aidogenic bactera enter, demineralise enamel and dentine 2nd wave colonisation of different bacteria mixed popilation produce proteolytic enzymes that destroy demineralisaed collagen matrix

what do bacteria do in the dentine tubules

mulitply in the tubules which widen and collapse | 'liquefaction foci'

what does collapsing of dentine tubles lead to

expansion and formation of dentine clefts | thes can flake off (point of weakness)

what is the body of the lesion subdivied into

demineralisation bacterial penetration destruction

what is in the demineralisation part of the body of the cavitation

dentine has lost mineral but still has tubular structure | no bacteria and dentine is stained

what is in the bacteria penetration of the body

bacteria multiply in tubles infected soft dentine stil maintains some tubular matrix

describe the destruction in the body

base of cavity discoloured liquefaction foci and transverse clefts

where is the head of the scleotic zone

near the pulp

what happens to the pulp upon caries advancing

pulp tries to shrink away from caries odontoblasts wrking hrder to make dentine more quickly tertiary dentine increasing in irregularity pulp inflammation increases bacteria invade tertiary dentine and reach pulp